During the 2009 fiscal year, we accomplished the following: 1. Completed the first phase of analysis of pulsed-BCR signaling in splenic B cells. We found that a single round of BCR signaling primed cells to receive T cell help by: i) secreting T cell attracting chemokines CCL3 and CCL4; ii) up-regulating the chemokine receptor CCR7 that facilitates B cell migration to T cell zones; iii) up-regulating MHC II surface expression;and iv) increasing the sensitivity to CD40 signals. 2. The basis for hyper-responsiveness to CD40 was proposed to be due to down-regulation of the adapter molecule, BANK, which is a negative regulator of CD40. In addition, CD40 responsiveness was reduced in c-Rel-deficient B cells indicating that a part of the priming effect was mediated via this NF-kB family member. 3. Initiated a collaboration with Dr. Mark Shlomchik to determine whether pulse activation occurs during in vivo immunization. Enroute to the in vivo experiment, we showed that antigen-specific priming occurs in vitro. 4 Completed the first phase of analysis of the function of two phases of c-Rel induction in BCR-activated spleen B cells in collaboration with Dr. Steve Gerondakis. We found that phase l c-Rel induces A1 gene expression and phase 2 c-Rel induces Bcl-XL gene expression. Both A1 and Bcl-XL were found to be important to maintain B cell viability after BCR cross-linking.